Chorioamnionitis Clinical Presentation

Updated: May 08, 2018
  • Author: Fayez M Bany-Mohammed, MD; Chief Editor: Ted Rosenkrantz, MD  more...
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Presentation

History

The time-honored clinical signs and symptoms of chorioamnionitis include the following:

  • Intrapartum fever: The National Institute of Child Health and Human Development (NICHD) workshop report defined maternal fever as temperature of at least 39.0°C [102.2°F] or 38.0°C [100.4°F] to 38.9°C [102.02°F] on two occasions 30 minutes apart, [1] without another clear source. [2]
  • Significant maternal tachycardia (>120 beats per minute [bpm])
  • Base line fetal tachycardia (>160 bpm for 10 min or longer, excluding accelerations, decelerations, and periods of marked variability)
  • Maternal leukocytosis (total blood leukocyte count >15,000 cells/μL) in the absence of corticosteroids
  • Purulent-appearing fluid coming from the cervical os, as visualized by speculum examination
  • Other nonspecific signs such as maternal tachycardia and uterine tenderness are deemphasized by the NICHD. [2]

Of these criteria, intrapartum maternal fever appears to be the most frequent and necessary to make the diagnosis of intrauterine infection according to the workshop conducted by NICHD [2] and later endorsed by the American College of Obstetricians and Gynecologists (ACOG). [30] According to this report, women who have fever without other chorioamnionitis symptoms or signs are regarded as having “isolated fever” and should not be diagnosed as having chorioamnionitis or “triple I.” Additionally, the NICHD report deemphasized nonspecific signs like uterine tenderness, maternal tachycardia, and vaginal discharge because some of these signs occur during the normal course of physiologic labor or can be masked by neuraxial anesthesia. Of note, for treatment purposes, ACOG further suggests that patients with isolated fever of at least 39.0°C (102.2°F) should be managed as having suspected intraamniotic infection. [30]

When at least two of the aforementioned criteria are present, the risk of neonatal sepsis is increased. Each clinical sign and symptom of chorioamnionitis, however, is by itself of low predictive value. The signs and symptoms of maternal chorioamnionitis are so subjective and the term “chorioamnionitis,” which should be reserved to describe histologic changes in the placenta and membranes, has been used widely by clinicians, sometimes to describe isolated intrapartum low-grade fever. This has led to too many asymptomatic newborns being evaluated for early-onset sepsis (EOS) and being unnecessarily exposed to antibiotics, with significant variations in practice among neonatal intensive care unitis (NICUs). [121] The NICHD workshop expert panel report, even though not considered a formal consensus recommendation by the NICHD, is a step in the right direction to define the problem and recommend a unified approach for diagnosis and management of chorioamnionitis, both for obstetric and neonatal care providers.

The NICHD workshop recommended using the term “triple I” to address the heterogeneity of this disorder. The term "triple I" refers to intrauterine infection or inflammation or both, and it is defined by strict diagnostic criteria (see Diagnostic Considerations); however, this terminology has not been universally accepted. [3] It is important to differentiate between clinical and histologic chorioamnionitis; the latter tend to be “silent” and present only with preterm labor or preterm premature rupture of membranes (PPROM). The risk of neonatal sepsis is increased when chorioamnionitis is diagnosed in the laboring mother; however, the risk is much lower than anticipated based on historical figures when widespread use of intrapartum antibiotics was not a common practice. [4]

An increasing or decreasing total leukocyte count may be more important than a single determination. Abnormalities in either umbilical vein interleukin (IL)-6 levels or an increasing neonatal immature-to-total neutrophil ratio, along with clinical criteria associated with chorioamnionitis, improve the sensitivity and predictive accuracy of identifying the septic neonate.

Although many cytokines and inflammatory markers have been proposed as diagnostic tests for EOS in the newborn, none has been of sufficient predictive value to gain wide acceptance. [10, 122, 123] Some cytokines are only secreted over a limited time frame during the start of infection, and inflammatory markers may be more sustained in their presence. Levels of C-reactive proteins (CRPs) are useful to exclude infection and discontinue antibiotics. Some investigators suggest that using a combination of markers like CRP, procalcitonin, IL-6, presepsin (soluble CD14 subtype), in conjunction with other cell-surface antigens such as CD11b, CD64, and human leukocyte antigen-antigen D related (HLA-DR) may enhance the laboratory diagnosis of EOS. [124, 125, 126]

Next:

Physical Examination

The diagnosis of clinical chorioamnionitis in pregnancy is commonly made based on clinical findings of fever plus fetal tachycardia, maternal leukocytosis, or purulent fluid coming from the cervical os. Additionally, the pregnant woman with chorioamnionitis may appear ill, even toxic, and she may exhibit hypotension, diaphoresis, and/or cool or clammy skin. However, especially when dealing with histologic chorioamnionitis, maternal clinical signs or symptoms of infection may be absent (silent chorioamnionitis). [5]

Furthermore, clinical signs and symptoms of chorioamnionitis are not always associated with placental evidence of inflammation. [6] This is particularly true if maternal fever is the sole criterion for the diagnosis.

Examination for suspected sepsis in a woman with chorioamnionitis may include the following findings:

  • Fever
  • Tachycardia (>120 bpm)
  • Hypotension
  • Diaphoresis
  • Cool or clammy skin
  • Uterine tenderness
  • Foul-smelling or purulent vaginal discharge

The presence of intraamniotic amniotic fluid "sludge," a free-floating hyperechogenic material within the amniotic fluid in close proximity to the uterine cervix, reflects intraamniotic inflammation with or without microorganisms. [127]  On uterine ultrasonography, this finding has been seen in asymptomatic women at risk for preterm delivery. [12, 128]  More recent studies confirm that amniotic fluid sludge is a useful marker of microbial invasion of the amniotic cavity, histologic chorioamnionitis, and funisitis—conditions that increase the risk for preterm delivery at an extreme gestational age. [129]  Aseptic aspiration of the "sludge" may show the material to have a low glucose content, many neutrophils, and organisms such as gram-positive cocci or Candida. [130, 128]

Clinical signs and symptoms of chorioamnionitis are not always associated with placental evidence of inflammation. [66] This is particularly true if maternal fever is the sole criterion for the diagnosis.

Epidural anesthesia during the intrapartum period has been associated with fever in the mother and the neonate [131, 132] ; a primary sterile inflammatory response either in the placenta or in the epidural space (with secondary inflammation in the placenta and chorioamniotic membranes) is the most likely etiology. [67, 68, 133]  Other etiologic factors in epidural anesthesia-induced fever include nulliparity, dysfunctional labor, prolonged labor, maternal exhaustion, dehydration, and/or prolonged rupture of membranes. [134]

Because it is hard to differentiate epidural anesthesia-induced maternal fever from intraamniotic infection, maternal and/or neonatal fevers result in more evaluations for sepsis and antibiotic treatment in neonates. [135] In addition to the risk for unnecessary exposure to antibiotics, fever itself may be damaging to the newborn, especially in the setting of hypoxia-ischemia. [136]

In the setting of epidural anesthesia during labor, the following clinical course has been observed. The fetus usually has tachycardia when the mother is febrile during labor. At birth, the newborn may also have a fever (temperature >38.0ºC [100.4ºF]). If the neonate is not septic, the temperature elevation dissipates rapidly following birth, and the newborn subsequently exhibits normal behavior. Usually a temperature elevation in the neonate has returned to normal within 30-60 minutes after birth. Furthermore, these noninfected, febrile neonates have normal Apgar scores and appear remarkably well following birth. Such newborns can be observed for illness rather than undergo a septic workup and antibiotic therapy. However, clinical judgment must be based on many factors, including the intrapartum administration of broad-spectrum antibiotics to the mother.

Examination for suspected sepsis in the neonate of a mother with chorioamnionitis often yields nonspecific and subtle findings, which may include the following:

  • Behavioral abnormalities (eg, lethargy, hypotonia, weak cry, poor suck)
  • Pulmonary: Tachypnea, respiratory distress, cyanosis, pulmonary hemorrhage, and/or apnea
  • Cardiovascular: Tachycardia, hypotension, prolonged capillary refill time, cool and clammy skin, pale or mottled appearance, and/or oliguria
  • Gastrointestinal: Abdominal distention, vomiting, diarrhea, and/or bloody stools
  • Central nervous system (CNS): Thermal regulatory abnormalities, behavioral abnormalities, apnea, and/or seizures
  • Hematologic and/or hepatic: Pallor, petechiae or purpura, and overt bleeding

The fetus may have tachycardia (>160 bpm) or decreased variability. [137]  A biophysical profile (BPP) performed on the fetus using ultrasonography may reveal a lower than normal score, but ultrasonic biophysical profile assessment has not been predictive of clinical chorioamnionitis. [138]  Lack of fetal breathing has been associated with fetal infection. [139, 140]

Tachypnea, respiratory distress (eg, expiratory grunt, retractions), cyanosis, pulmonary hemorrhage, and/or apnea (ie, pulmonary manifestations of pneumonia, sepsis, or both), must be immediately appreciated by caregivers. Nursery personnel must be aware that a neonate who is born without respiratory distress but who develops signs and symptoms of pulmonary disease in the first 6-12 hours of life has a heightened risk for congenital (infectious) pneumonia.

Tachycardia, hypotension, prolonged capillary refill time, cool and clammy skin, pale or mottled appearance, oliguria (ie, cardiovascular manifestations of sepsis), or a combination of these may be observed, typically occurring late in the course of early-onset sepsis (EOS). Caregivers must also consider other explanations for these physical findings, such as developmental defects in the cardiovascular system (ie, cardiovascular malformations with abnormalities of aortic blood flow) or inborn errors of metabolism.

Gastrointestinal symptoms, as outline above, may be nonspecific in patients with EOS.

Thermal regulatory abnormalities (ie, hypothermia or hyperthermia), behavioral abnormalities, apnea, seizures (ie, CNS manifestations), or a combination may be seen. A bulging fontanel or nuchal rigidity is not a reliable sign of meningitis in a neonate.

Pallor, petechiae or purpura, and overt bleeding (ie, hematopoietic involvement, liver involvement, or both) may be seen and requires immediate diagnostic and therapeutic attention.

Because one physiologic system may affect another, signs and symptoms may originate from more than one dysfunctional organ. However, many neonatal conditions resemble neonatal sepsis; thus, physician caregivers must have an open mind regarding other clinical conditions that may involve signs and symptoms resembling those of neonatal sepsis. Those conditions include, but are not limited to, the following:

  • Cardiovascular malformations, especially left-sided obstructive lesions causing poor systemic cardiac output
  • Endocrine disorders that may also cause shocklike states, such as different types of congenital adrenal insufficiency or hypoglycemia associated with hyperinsulinemia
  • Serious CNS trauma or dysfunction from any cause and subtle seizures with systemic manifestations
  • Anemia caused by unrecognized isoimmunization or blood loss from conditions such as fetomaternal transfusion syndrome
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